Monopoly Market with Externality: an Analysis with Statistical Physics and ACE

In this paper, we explore the effects of localised externalities introduced through interaction structures upon the properties of the simplest market model: the discrete choice model with a single homogeneous product and a single seller (the monopoly case). The resulting market is viewed as a complex interactive system with a communication network. Our main goal is to understand how generic properties of complex adaptive systems can enlighten our understanding of the market mechanisms when individual decisions are inter-related. To do so we make use of an ACE (Agent based Computational Economics) approach, and we discuss analogies between simulated market mechanisms and classical collective phenomena studied in Statistical Physics. More precisely, we consider discrete choice models where the agents are subject to local positive externality. We compare two extreme special cases, the McFadden (McF) and the Thurstone (TP) models. In the McF model the individuals' willingness to pay are heterogeneous, but remain fixed. In the TP model, all the agents have the same homogeneous part of willingness to pay plus an additive random (logistic) idiosyncratic characteristic. We show that these models are formally equivalent to models studied in the Physics literature, the McF case corresponding to a `Random Field Ising model' (RFIM) at zero temperature, and the TP case to an Ising model at finite temperature in a uniform (non random) external field. From the physicist's point of view, the McF and the TP models are thus quite different: they belong to the classes of, respectively,`quenched' and `annealed' disorder, which are known to lead to very different aggregate behaviour. This paper explores some consequences for market behaviour. Considering the optimisation of profit by the monopolist, we exhibit a new `first order phase transition': if the social influence is strong enough, there is a regime where, if the mean willingness to pay increases, or if the production costs decreases, the optimal solution for the monopolist jumps from a solution with a high price and a small number of buyers, to a solution with a low price and a large number of buyers.Agent-Based Computational Economics, discret choices, consumers externality, complex adaptive system, phase transition, avalanches, interactions, hysteresis.

Cohomology of the Lie Superalgebra of Contact Vector Fields on R1∣1\mathbb{R}^{1|1} and Deformations of the Superspace of Symbols

Following Feigin and Fuchs, we compute the first cohomology of the Lie superalgebra $\mathcal{K}(1)$ of contact vector fields on the (1,1)-dimensional real superspace with coefficients in the superspace of linear differential operators acting on the superspaces of weighted densities. We also compute the same, but $\mathfrak{osp}(1|2)$-relative, cohomology. We explicitly give 1-cocycles spanning these cohomology. We classify generic formal $\mathfrak{osp}(1|2)$-trivial deformations of the $\mathcal{K}(1)$-module structure on the superspaces of symbols of differential operators. We prove that any generic formal $\mathfrak{osp}(1|2)$-trivial deformation of this $\mathcal{K}(1)$-module is equivalent to a polynomial one of degree $\leq4$. This work is the simplest superization of a result by Bouarroudj [On $\mathfrak{sl}$(2)-relative cohomology of the Lie algebra of vector fields and differential operators, J. Nonlinear Math. Phys., no.1, (2007), 112--127]. Further superizations correspond to $\mathfrak{osp}(N|2)$-relative cohomology of the Lie superalgebras of contact vector fields on $1|N$-dimensional superspace

On sl(2)-equivariant quantizations

By computing certain cohomology of Vect(M) of smooth vector fields we prove that on 1-dimensional manifolds M there is no quantization map intertwining the action of non-projective embeddings of the Lie algebra sl(2) into the Lie algebra Vect(M). Contrariwise, for projective embeddings sl(2)-equivariant quantization exists.Comment: 09 pages, LaTeX2e, no figures; to appear in Journal of Nonlinear Mathematical Physic

Atomic Dark Matter

We propose that dark matter is dominantly comprised of atomic bound states. We build a simple model and map the parameter space that results in the early universe formation of hydrogen-like dark atoms. We find that atomic dark matter has interesting implications for cosmology as well as direct detection: Protohalo formation can be suppressed below $M_{proto} \sim 10^3 - 10^6 M_{\odot}$ for weak scale dark matter due to Ion-Radiation interactions in the dark sector. Moreover, weak-scale dark atoms can accommodate hyperfine splittings of order 100 \kev, consistent with the inelastic dark matter interpretation of the DAMA data while naturally evading direct detection bounds.Comment: 17 pages, 3 figure

Real-Time Hemodynamic Evidence Supporting the Safety of Acute Isometric Exercise

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Kvalitativna procjena eliminacije TCP-a i TAMORF-a iz organizma štakora metodom GC-MS

Nerve agents are highly toxic organophosphorus (OP) compounds. They inhibit acetylcholinesterase (AChE), an enzyme that hydrolyses acetycholine (ACh) in the nervous system. Pathophysiological changes caused by OP poisonings are primarily the consequence of surplus ACh on cholinergic receptors and in the central nervous system. Standard treatment of OP poisoning includes combined administration of carbamates, atropine, oximes and anticonvulsants. In order to improve therapy, new compounds have been synthesised and tested. Tenocyclidine (TCP) and its adamantane derivative 1-[2-(2-thienyl)-2-adamantyl] morpholine (TAMORF) have shown interesting properties against soman poisoning. In this study, we developed a qualitative GC-MS method to measure elimination of TCP and TAMORF through rat urine in order to learn more about the mechanisms through which TCP protects an organism from OP poisoning and to determine the duration of this protective effect. GC-MS showed that six hours after treatment with TCP, rat urine contained only its metabolite 1-thienylcyclohexene, while urine of rats treated with TAMORF contained both TAMORF and its metabolites.Živčani bojni otrovi po strukturi su organofosforni (OP) spojevi, čija je zajednička značajka ireverzibilna inhibicija acetilkolinesteraze (AChE), enzima koji hidrolizira acetilkolin (ACh) u živčanom sustavu. Patofi ziološka zbivanja koja nastaju pri otrovanju OP-spojevima primarno su posljedica akumuliranog ACh na kolinergičkim receptorima i u središnjem živčanom sustavu. Još uvijek nesavršen, standardni tretman liječenja otrovanja OP-spojevima uključuje kombiniranu primjenu estera karbamata, atropina, oksima i antikonvulziva. Kako bi se unaprijedila uobičajena terapija, osobito kod otrovanja somanom, ispituju se antidotski učinci mnogih spojeva. Tenociklidin (TCP) i njegov adamantanski derivat TAMORF pokazali su zanimljiva svojstva pomoćne terapije pri otrovanju somanom. Kako bi se proširile dosadašnje spoznaje o načinu na koji tenociklidini štite organizam od trovanja OP-spojevima te također o trajanju njihova antidotskog učinka, u ovom radu razvijena je GC-MS-metoda za praćenje eliminacije TCP-a i TAMORF-a iz organizma. Rezultati GC-MS-analize pokazali su da šest sati nakon tretiranja štakora TCP-om mokraće sadržavaju metabolit TCP-a 1-tienilcikloheksen, dok šest sati nakon tretiranja štakora TAMORF-om mokraće sadržavaju i TAMORF i njegove metabolite. Drugim riječima, šest sati nakon tretmana TCP se potpuno metabolizira, dok se TAMORF metabolizira djelomično, a djelomično ostaje nepromijenjen

US Cosmic Visions: New Ideas in Dark Matter 2017: Community Report

This white paper summarizes the workshop "U.S. Cosmic Visions: New Ideas in Dark Matter" held at University of Maryland on March 23-25, 2017.Comment: 102 pages + reference

TAFRO syndrome: New subtype of idiopathic multicentric Castleman disease

Castleman disease (CD) describes a group of three rare and poorly understood lymphoproliferative disorders that have heterogeneous clinical symptoms and common lymph node histopathological features. Unicentric CD (UCD) involves a single region of enlarged nodes. Multicentric CD (MCD) involves multiple regions of enlarged lymph nodes, constitutional symptoms, and organ dysfunction due to a cytokine storm often including interleukin 6. MCD is further divided into Human Herpes Virus-8 (HHV-8)-associated MCD, which occurs in immunocompromised individuals, and HHV-8-negative/idiopathic MCD (iMCD). Recently, iMCD has been further sub-divided into patients with TAFRO syndrome, which involves thrombocytopenia (T), anasarca (A), fevers (F), reticulin myelofibrosis (R), organomegaly (O), and normal or only slightly elevated immunoglobulin levels, and those who do not have TAFRO syndrome. Non-TAFRO iMCD patients typically have thrombocytosis, less severe fluid accumulation, and hypergammaglobulinemia. iMCD patients with TAFRO syndrome may have a worse prognosis, but more research is needed

Kinome rewiring reveals AURKA limits PI3K-pathway inhibitor efficacy in breast cancer.

Dysregulation of the PI3K-AKT-mTOR signaling network is a prominent feature of breast cancers. However, clinical responses to drugs targeting this pathway have been modest, possibly because of dynamic changes in cellular signaling that drive resistance and limit drug efficacy. Using a quantitative chemoproteomics approach, we mapped kinome dynamics in response to inhibitors of this pathway and identified signaling changes that correlate with drug sensitivity. Maintenance of AURKA after drug treatment was associated with resistance in breast cancer models. Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo. This signaling map identifies survival factors whose presence limits the efficacy of targeted therapies and reveals new drug combinations that may unlock the full potential of PI3K-AKT-mTOR pathway inhibitors in breast cancer

Reduced skeletal muscle protein balance in paediatric Crohn’s disease

Background and AimsAn inability to respond to nutrition could be implicated in low muscle mass in Crohn’s disease. We aim to determine skeletal muscle metabolic response to feeding in Crohn’s disease and healthy volunteers.MethodsTwenty asymptomatic Crohn’s disease participants (15.6 ± 0.5 yrs; BMI 20.6 ± 0.9 kg/m2); 9 with active disease (faecal calprotectin, 808 ± 225ug/g and C-reactive protein, 2.2 ± 1.2 mg/dl), 11 in deep remission (faecal calprotectin, 61 ± 12ug/g and C-reactive protein, 0.3 ± 0.2 mg/dl) and 9 matched healthy volunteers (16.0±0.6 yrs; BMI 20.7±0.6 kg/m2) were recruited. Participants had a dual energy X-ray absorptiometry scan, handgrip dynamometer test, wore a pedometer and completed a food diary. Arterialised hand and venous forearm blood samples were collected concurrently and brachial artery blood flow measured at baseline and every 20mins for 2hrs after the ingestion of a standardised liquid meal. Net balance of branched chain amino acids and glucose were derived.ResultsControls had a positive mean BCAA balance. CD participants had an initial anabolic response to the meal, with increasing BCAA balance between t=0 & t=20, but returned to negative by t=60. This was associated with reduced FFM z-scores in CD but not with insulin resistance or disease activity. Exploratory analyses suggest that negative postprandial BCAA response seen in CD is predominant in males (p=0.049), with associated lower appendicular muscle mass (p=0.034), higher muscle fatigue (p=0.014) and reduced protein intake (p=0.026).ConclusionsThe inability to sustain a positive protein balance postprandially could provide an explanation for the reduced muscle mass seen in CD. Further mechanistic studies will be needed to confirm these findings